Article(id=1276975994275762659, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276975955985961244, articleNumber=null, orderNo=null, doi=10.19540/j.cnki.cjcmm.20251011.702, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1755705600000, receivedDateStr=2025-08-21, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1782384402102, onlineDateStr=2026-06-25, pubDate=1767196800000, pubDateStr=2026-01-01, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1782384402102, onlineIssueDateStr=2026-06-25, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1782384402102, creator=13701087609, updateTime=1782384402102, updator=13701087609, issue=Issue{id=1276975955985961244, tenantId=1146029695717560320, journalId=1276577828834349082, year='2026', volume='51', issue='1', pageStart='1', pageEnd='300', issueExtLink='null', onlineDate='null', pubDate='1767196800000', pubDateStr='2026-01-01', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1782384392973, creator='13701087609', updateTime=1782384484405, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1276976339546673871, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276975955985961244, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1276976339546673872, tenantId=1146029695717560320, journalId=1276577828834349082, issueId=1276975955985961244, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=181, endPage=190, ext={EN=ArticleExt(id=1276975994581946853, articleId=1276975994275762659, tenantId=1146029695717560320, journalId=1276577828834349082, language=EN, title=Sculponeatin A inhibits growth and induces apoptosis of triple-negative breast cancer cells by targeting c-Myc/CIP2A axis, columnId=null, journalTitle=Chinese Journal of Traditional Chinese Medicine, columnName=null, runingTitle=null, highlight=null, articleAbstract=

This article aims to investigate the inhibitory effect and molecular mechanism of sculponeatin A (STA) on triple negative breast cancer (TNBC). MDA-MB-436 and MDA-MB-468 were selected as cell models. The MTT assay, real-time cell analysis (RTCA), and colony formation assay were used to evaluate the effects of different concentrations of STA on the proliferation of TNBC cells. JC-1 staining and Annexin V-FITC/PI double staining combined with flow cytometry were used to measure the effect of STA on the apoptosis of TNBC cells. Western blot was employed to determine the expression changes of apoptosis-related proteins [cysteinyl aspartate-specific proteinase (caspase)-9, caspase-3, and poly-ADP-ribose polymerase (PARP)] and cancerous inhibitor of protein phosphatase 2A (CIP2A)/protein kinase B (AKT) signaling pathway proteins [CIP2A, AKT, phosphorylated (p)-AKT] in TNBC cells after STA treatment. To clarify the function of CIP2A in the action of STA, a CIP2A overexpression or CIP2A knockdown plasmid was transfected into cells, which were then treated with STA. Cell proliferation, apoptosis, and protein expression changes were evaluated by CCK-8, flow cytometry, and Western blot. Further, RT-qPCR and Western blot both showed that STA significantly downregulated the mRNA and protein levels of CIP2A and the protein level of c-Myc. The overexpression of c-Myc antagonized the downregulating effects of STA on the protein and mRNA levels of CIP2A, while the knockdown of c-Myc enhanced this effect. The drug affinity-responsive target stability (DARTS) assay and microscale thermophoresis (MST) assay confirmed the existence of direct binding between STA and c-Myc protein. The results indicated that STA significantly inhibited the proliferation and colony formation and induced the apoptosis of TNBC cells, manifested by an increased apoptosis rate, downregulated precursor protein expression of caspase-9 and caspase-3, and increased PARP cleavage. STA treatment reduced the p-AKT level but did not affect total AKT. Functionally, the knockdown of CIP2A enhanced the STA effects of inhibiting proliferation and inducing apoptosis, while the overexpression of CIP2A produced antagonistic effects. From a mechanism perspective, STA directly targets and binds to c-Myc to downregulate its expression, thereby inhibiting the transcription and translation of CIP2A and ultimately blocking the c-Myc/CIP2A signaling pathway. In conclusion, STA inhibits the malignant progression of TNBC by targeting the c-Myc/CIP2A signaling axis.

, authors=null, authorsList=Song-ran SHENG, Xu ZHANG, Liang ZHANG, Chen QIAN, Yuan SI, authorCompany=null, correspAuthors=Yuan SI, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1276975995001377256, articleId=1276975994275762659, tenantId=1146029695717560320, journalId=1276577828834349082, language=CN, title=黄花香茶菜甲素靶向c-Myc/CIP2A轴抑制三阴性乳腺癌生长及诱导凋亡的作用机制, columnId=1276975994707775974, journalTitle=中国中药杂志, columnName=药理, runingTitle=null, highlight=null, articleAbstract=

该文旨在探究黄花香茶菜甲素（STA）对三阴性乳腺癌（TNBC）的抑制作用及分子机制。选用MDA-MB-436、MDA-MB-468细胞作为模型。通过MTT法、实时无标记细胞分析技术（RTCA）和克隆形成实验检测不同浓度STA对TNBC细胞增殖能力的影响；JC-1染色和Annexin V-FITC/PI双染结合流式细胞术检测STA对TNBC细胞凋亡的影响。蛋白免疫印迹法检测STA对TNBC细胞相关凋亡蛋白天冬氨酸特异性半胱氨酸蛋白酶（caspase）-9、caspase-3和聚腺苷二磷酸核糖聚合酶（PARP）及蛋白磷酸酶2A癌性抑制因子（CIP2A）/蛋白激酶B（AKT）信号通路蛋白CIP2A、AKT、磷酸化蛋白激酶B（p-AKT）的表达变化。为明确CIP2A在STA作用中的功能，在细胞中过表达或敲减CIP2A质粒，结合STA处理，通过CCK-8、流式细胞术和Western blot评估细胞增殖、凋亡及相关蛋白的变化。进一步RT-qPCR和Western blot结果均显示STA显著下调CIP2A的mRNA及蛋白水平，STA亦下调c-骨髓细胞瘤病病毒癌基因同源物（c-Myc）蛋白表达；过表达c-Myc可拮抗STA对CIP2A蛋白和mRNA水平的下调作用，而敲减c-Myc则增强此效应。靶点稳定性的药物亲和反应实验（DARTS）和微量热泳动实验（MST）证实STA与c-Myc蛋白存在直接结合。结果表明STA能显著抑制TNBC细胞增殖与克隆形成，并诱导细胞凋亡，表现为凋亡比例升高，caspase-9和caspase-3前体蛋白表达下调及PARP切割增加。STA处理降低p-AKT水平，但不影响总AKT。功能上，敲减CIP2A增强STA的抑增殖和促凋亡作用，而过表达CIP2A则产生拮抗效应。机制上，STA通过直接靶向结合c-Myc，下调其表达，进而抑制CIP2A转录与翻译，最终阻断c-Myc/CIP2A信号通路。综上表明，STA通过靶向c-Myc/CIP2A信号轴抑制TNBC恶性进展。

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